Activity dependent plasticity Flashcards

1
Q

how many layers does the neocortex have

A

6 layers

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2
Q

what is layer IV

A

thalamo-recipient layer

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3
Q

prey vs predator visual anatomy

A

prey = eyes on side
predator = eyes on the front

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4
Q

visual system route

A

retina
LGN
striate cortex (IV)

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5
Q

what stains retinotopic maps

A

cytochrome oxidase

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6
Q

what does optical imaging measure for

A

amount of oxygenated blood (activity)

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7
Q

Sur, Garraghty & Roe (1988)
Turning auditory cortex into visual cortex (Ferret)

A

lesion collicular pathway
loss of auditory input to MGN
feed optic nerve into LGN and MGN
develops orientation specific neurons in A1 which respond to visual features

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8
Q

what is hebbian plasticity

A

modification of existing connections between neurons

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9
Q

criteria to implement hebbian plasticity

A

activity dependence between pre and post synaptic neurons

input specificity (inputs co-active with post synaptic cells)

cooperativity (multiple inputs at once)

associativity (info from 2 sources can be integrated)

longevity (change should last for a specific period)

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10
Q

long term potentiation LTP

A

artificial hebbian plasticity
tetanus (100Hz) causes LTP

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11
Q

(beck at el., 2000)
Input specificity of LTP

A

Insert 2 electrodes in human hippocampal slice (DG)
Input 1 - baseline and tetanus causes LTP after high frequency stimulation
Input 2 - baseline only

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12
Q

AMPA receptor

A

ionotropic glutamate receptor which allows Na+ ion influx via electrostatic and diffusion movement

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13
Q

AMPA R antagonist

A

CNQX

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14
Q

NMDA receptor

A

coincidence detector/induction mechanism

It is ligand and voltage gated
Blockade via Mg2+ in pore
depolarisation removes Mg2+ blockade
NMDAR antagonist (AP5/APV) blocks LTP induction

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15
Q

LTD features

A

LTD is input specific and dependent on NMDAR like LTP
(fire out of sync lose your link)

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16
Q

HFS/LFS of the post synaptic cell

A

HFS - temporal summation - high 5um Ca2+ - protein kinases increase AMPAR function
LFS - low 1um Ca2+ - protein phosphatase decrease AMPAR function

overstimulation can cause epilepsy/coma

17
Q

ocular dominance

A

contralateral and ipsilateral inputs segregated in L4 (binocular vision requires C&I integration)
ocular dominance occurs in L4 of primate/striate cortex
autoradiography tracks ocular dominance (retina-LGN-striate cortex)

18
Q

methods to inactivate the retina

A

Colombian tree frog (epibatidine)
newts and pufferfish/fugu - tetrodotoxin TTX - blocks VGSC
Huberman et al., 2003 - normal eye opening occurs at p1-10 in ferret - segregation occurs in LGN, epibatidine inactivates the retina and causes blurred segregation
spontaneous activity not correlated between the two retina

19
Q

what is needed for segregation zones in mouse SI

Iwasato et al., 2000

A

NMDAR
CXNR1 KO causes no whisker barrel formation

20
Q

Hubel & Wiesel
monocular deprivation in kittens

A

monocular deprivation of contralateral eye - open contralateral eye - almost all neurons responsive to ipsilateral eye
strabismus (squint) of contralateral eye - equal distribution of responsive neurons
monocular deprivation of contralateral eye - open contralateral eye and NMDAR blockade - no OD shift

therefore, monocular deprivation causes a shift in organisation in LGN & L4 of V1, LTD like plasticity (use it or lose it)

21
Q

ganglion cell receptive field

A

centre - positive maximal activity
surround - negative minimal activity
ganglion cells differ in firing APs

22
Q

orientation selectivity

A

orientation selectivity to experience dependence (Ca2+ dependence) - blocked by NMDAR antagonist APV
feedforward excitation from LGN relay cells and summate to form orientation selectivity and intracortical lateral inhibition

23
Q

critical period
monocular deprivation in cats

A

5wks (OD shift is reversible in kittens) - monocular deprivation of the contralateral eye and reverse suture - close ipsilateral eye- recovers binocular dominance in contralateral eye

14wks - no plasticity (critical period is closed) recently closed ipsilateral eye is dominant

24
Q

cortical inhibition and the critical period

A

low cortical inhibition - no plasticity
high cortical inhibition - critical period closes
feedforward GABA inhibition is needed to open the critical period
little inhibition = improper coding = no OD plasticity (hence no critical period)

25
Q

Human Amblyopia

A

lazy eye - cortical blindness
reduced visual acuity in otherwise healthy and properly corrected eye
no depth perception- prevents employment
2% of UK population is affected
most common cause of vision loss

26
Q

causes of amblyopia

A

strabismus
cataracts/corneal surgery
anisometropia (differences in the refractive index)

27
Q

amblyopia treatment

A

patch/atropine eyedrops (punish good eye)
-gain in amblyopic eye in expense of fellow eye
-little/no improvement in binocular vision
-poor compliance & varied outcome
-only effective in early childhood

28
Q

temporary monocular deprivation in cats
amblyopia

A

deficits in binocular vision is restored
10 days of dark exposure recovers eye depression in cats and fluoxetine (prozac) SSRI antidepressant restores critical period plasticity via reduced inhibition, reopens critical period

29
Q

synaptic scaling experiment

Turrigiano & Nelson, 2004

A

TTX/CNQX then wash - hyperexcitation
bicuculline then wash - little innervation

potentiation follows depression - requires NMDAR

30
Q

Bienenstock, Cooper & Munro (BCM) theory of synaptic plasticity

A

reduced cortical activity = reduced LTD and increased LTP
activity dependence = presynaptic neurons strengthens the synapse only if the postsynaptic neuron is activate (vice versa)